Thyroxine treatment increases the hypoxic pulmonary vasoconstriction in isolated lungs from thyroidectomized rats.

Abstract

The possibility that changes in energy metabolism are involved in oxygen sensing during hypoxic pulmonary vasoconstriction was tested indirectly by measurement of hypoxic-pressor reactivity in lungs isolated from rats with low and high levels of plasma thyroxine. In the first study, male rats were treated for one week after thyroidectomy with 50 micrograms (n = 6) or 100 micrograms (n = 6) thyroxine per 100 g body weight (b.w.) daily or with solvent (n = 6). The lungs were isolated and perfused at constant flow with salt-albumin solution. They were ventilated with air +5% CO2 in a humid chamber at 38 degrees C. The dose-pressor response to hypoxia and angiotensin II were measured. In the second study, thyroidectomized male rats were treated similarly with 100 micrograms thyroxine (n = 7) or solvent (n = 6) and isolated lungs were perfused with homologous blood obtained from thyroidectomized blood donors treated in the same manner. Then the dose-pressor responses to hypoxia and K+ were elicited. The hypoxic-pressor responses were bigger in thyroxine than in solvent-treated rats. The response to angiotensin II and K+ was not affected by thyroxine treatment. The results are consistent with the idea that hypoxic-pressor reactivity varies directly with the metabolic rate of lung tissue.